Low expression of miR-142-3p promotes intervertebral disk degeneration.
Low expression of miR-142-3p promotes intervertebral disk degeneration.
复制标题
MiR-142-3p低表达促进椎间盘退变。
DOI:
10.1186/s13018-020-02194-4
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发表时间:
2021-01-14
影响因子:
2.6
通讯作者:
Yang X
中科院分区:
文献类型:
--
作者:
Xue J;Hu B;Xing W;Li F;Huang Z;Zheng W;Wang B;Zhu Y;Yang X
Intervertebral disk degeneration (IDD) is a degenerative disease characterized by cytoplasm loss and extracellular matrix degradation. Numerous evidence reported that miRNAs participated in IDD development. Nevertheless, the function of miR-142-3p in IDD development remains unknown. This study mainly explored the potential role and function of miR-142-3p in IDD development. One percent fetal bovine serum was used to induce the degeneration of ATDC5 cells, and miR-142-3p level was examined by qRT-PCR. Then, miR-142-3p mimic/inhibitor and its corresponding negative control were transfected into ATDC5 normal and degenerative cells. Viability, migration, invasion, apoptosis, cycle, Bax, Bcl-2, P62, and Beclin1 expression levels were assessed using CCK8, wound healing assay, annexin V-FITC/PI staining, western blot, and qRT-PCR, respectively. The results revealed that the expression levels of MMP13, ADAMTS5, MMP3, and Col-X were increased as well as the expression levels of SOX-9 and Col-II were reduced in ATDC5 degenerative cells, indicating the degeneration model was constructed. We observed that miR-142-3p was decreased in ATDC5 degenerative cells and its suppression could promote ATDC5 cell degeneration. However, miR-142-3p overexpression could reverse the cell viability inhibition, as well as apoptosis and autophagy enhancement in ATDC5 degenerative cells. Our results proved that miR-142-3p may play an important role in disk degeneration. Further animal study is needed to illustrate the role of the miR-142-3p in IDD development. The online version contains supplementary material available at 10.1186/s13018-020-02194-4.
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影响因子:
7.4
作者:
Wu A;Dong W;Liu S;Cheung JPY;Kwan KYH;Zeng X;Zhang K;Sun Z;Wang X;Cheung KMC;Zhou M;Zhao J
通讯作者:
Zhao J
影响因子:
5.7
作者:
Winer A;Adams S;Mignatti P
通讯作者:
Mignatti P
影响因子:
4
作者:
Qiang, Jianhong;Lv, Tingting;Yang, Xichao
通讯作者:
Yang, Xichao
影响因子:
4
作者:
Wang, Jingjie;Liu, Xiaoyan;Sun, Yuanliang
通讯作者:
Sun, Yuanliang
影响因子:
4.2
作者:
Yamasaki, A;Itabashi, M;Nagai, N
通讯作者:
Nagai, N